My research is to examine the ability of human antibodies of the IgA class to ameliorate the inflammatory processes that are the hallmark of periodontal disease. It has been demonstrated that human IgA antibodies fail to activate the complement system, which has a major role in inflammation and in mediating the protective activities of other types of antibody. It has also been shown that human IgA antibodies interfere with complement activation by other antibodies or by the products of infectious agents themselves. This interference occurs with all forms of human IgA, but bacterial enzymes that remove carbohydrate components from IgA reverse the effect. In my project, I will be extending these studies to examine the interaction of human IgA antibodies with neutrophils which have receptors for IgA. Specific Aims: 1. To determine the presence and up/down regulation of receptors for the Fc of IgA FcaR on neutrophils in human gingivae. 2. To determine the consequences of stimulating these cells with different forms of human IgA, IgA immune complexes, or Fc fragments of IgA, with respect to release of inflammatory cytokines and proteases. 3. To assess the potential for periodontal damage caused by the release of these factors directly or acting through other gingival cells such as fibroblasts.